Low-Frequency Pulsed Magnetic Field Improves Depression-Like Behaviors and Cognitive Impairments in Depressive Rats Mainly via Modulating Synaptic Function.

Jiajia Yang,Ling Wang,Xiaoxuan Tang,Rong Liang,Chenguang Zheng,Dong Ming,Faqi Wang,Peng Zhou

doi:10.3389/fnins.2019.00820

Abstract

Transcranial magnetic stimulation (TMS) has shown great promise as a medical treatment of depression. The effectiveness of TMS treatment at high frequency has been well investigated; however, low-frequency TMS in depression treatment has rarely been investigated in depression-induced cognitive deficits. Herein, this study was carried out to assess the possible modulatory role of low-frequency pulsed magnetic field (LFPMF) on reversing cognitive impairment in a model of depression induced by chronic unpredictable stress (CUS). Wistar rats were randomly allocated into four groups as follows: a control group (CON), a control applied with LFPMF (CON + LFPMF), a CUS group, and a CUS treated with LFPMF (CUS + LFPMF) group. During 8 weeks of CUS, compared to those in the CON group, animals not only gained less weight but also exhibited anhedonia, anxiety, and cognitive decline in behavioral tests. After 2-week treatment of LFPMF, a 20 mT, 1 Hz magnetic stimulation, it reversed the impairment of spatial cognition as well as hippocampal synaptic function including long-term potentiation and related protein expression. Thus, LFPMF has shown effectively improvements on depressant behavior and cognitive dysfunction in CUS rats, possibly via regulating synaptic function.

Highlights

Depression is a major neuropsychological disorder and has the third-largest disease burden, with around 350 million patients suffering from it globally as of 2012 (Smith, 2014)
We indicate low-frequency pulsed magnetic field (LFPMF) (1 Hz) can ameliorate depressionlike behaviors and cognitive impairment in a model of depression induced by chronic unpredictable stress (CUS), as well as the potential mechanisms
The results showed that after the CUS procedure, the sucrose preference index (SPI) of the control group was significantly higher than that of the model group [Figure 2B, main effect of CUS model: F(1,25) = 108.153, p < 0.001, main effect of treatment: F(1,25) = 0.008, p = 0.929, no CUS model × treatment interaction: F(1,25) = 0.009, p = 0.925, two-way ANOVA], suggesting that CUS model rats behaved in anhedonia as depressive patients

Summary

Introduction

Depression is a major neuropsychological disorder and has the third-largest disease burden, with around 350 million patients suffering from it globally as of 2012 (Smith, 2014). It is a chronic disease and exhibits a wide variety of symptoms, such as depressive mood, sluggish ideation, and suicidal ideation (Pazini et al, 2016). Previous findings suggest that neuronal activity, neural plasticity, oxidative stress, and cortisol levels contribute to the pathogenesis of depression (Neylan et al, 2001; Bremner et al, 2004; Hassouna et al, 2016). Cognitive dysfunction refers to significant and persistent functional impairment, which has attracted increased attention in the treatment of depression

Methods

Results

Conclusion